Background Cognitive dysfunction has been recognized as a diabetes-related complication. Whether hyperglycemia or elevated fasting glucose are associated with cognitive decline remains controversial. We aimed to investigate the relationship between fasting glucose levels and cognitive function in diabetic and non-diabetic individuals. Methods Participants were Japanese diabetic (n = 191) and non-diabetic (n = 616) men, aged 46–81 years, from 2010–2014. Blood samples were taken after a 12 h fast. The Cognitive Ability Screening Instrument (CASI), with a maximum score of 100, was used for cognitive assessment. Cognitive domains of CASI were also investigated. Fractional logit regression with covariate adjustment for potential confounders was used to model cross-sectional relationships between fasting blood glucose and CASI score. Results For diabetic individuals, CASI score was 0.38 (95% confidence interval: 0.66–0.12) lower per 1 mmol/L higher fasting glucose level. Short-term memory domain also exhibited an inverse association. For non-diabetic individuals, a reverse U-shaped relationship was observed between fasting glucose and cognitive function, identifying a threshold for highest cognitive performance of 91.8 CASI score at 3.97–6.20 mmol/L (71.5–111.6 mg/dL) fasting glucose. Language ability domain displayed a similar relationship with fasting glucose. Conclusions Elevated fasting glucose levels in diabetic men were associated with lower cognitive function, in which short-term memory was the main associated domain. Interestingly, in non-diabetic men, we identified a threshold for the inverse relationship of elevated fasting glucose with cognitive function. Contrastingly to diabetic men, language ability was the main associated cognitive domain among non-diabetic men.

Abstract Background Patients with Brugada syndrome (BrS) are known to have arrhythmic events after alcohol drinking and are recommended to avoid its excessive intake. Mechanisms underlying the alcohol‐induced cardiac events are however unknown. This study aimed to test the hypothesis whether activity of alcohol‐metabolizing enzymes determines fatal arrhythmic events after drinking alcohol. Methods A total of 198 Japanese patients with BrS were enrolled in this study. These patients were classified into symptomatic (n = 90) and asymptomatic (n = 108) groups. The former was divided into an alcohol‐related group (syncope after alcohol drinking, n = 16) and an alcohol‐unrelated group (n = 74). Polymerase chain reaction was performed to determine genetic variants of genes encoding alcohol dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (ALDH2). Results The genotype distribution for ALDH2 was not significantly different between symptomatic and asymptomatic groups and between alcohol‐related and alcohol‐unrelated groups. The genotype distribution for ADH1B was not significantly different between symptomatic and asymptomatic groups, but the genotype ADH1B His/His was significantly more prevalent in the alcohol‐related group than in the alcohol‐unrelated group (81.3% vs 50%, P = .023). In multivariate logistic regression analysis, the genotype of ADH1B His/His was independently associated with syncope after alcohol drinking (odds ratio, 5.746; 95% confidence interval, 1.580‐28.421; P = .007). Conclusions Arrhythmic events after alcohol drinking was associated with enhanced activity of alcohol‐metabolizing enzyme ADH1B in our cohort of BrS. Therefore, the lifestyle change to avoid the excessive alcohol intake deserves attention.

Aims: Calcification in the coronary and aortic arteries has been linked to cardiovascular morbidity and mortality. The pathophysiological influence of aortic artery calcification (AAC) differs from that of coronary artery calcification (CAC). We aimed to compare the relationships between CAC and AAC and cardiovascular disease (CVD) risk factors. Methods: We examined a random sample of 1035 Japanese men aged 40-79 years. CAC and AAC were measured by computed tomography and scored according to the Agatston method. Using a logistic regression, we calculated the odds ratio (OR) as being in the highest quintile (Q5) of the calcification score compared to the lower quintiles (Q1-Q4) per 1 standard deviation higher CVD risk factor. Models were simultaneously adjusted for age, body mass index (BMI), systolic blood pressure, smoking (pack-year), alcohol intake, hemoglobin A1c, uric acid, estimated glomerular filtration rate (eGFR), serum lipids, and C-reactive protein. Differences in ORs were investigated using a generalized estimating equation. We performed a multiple linear regression using log-transformed CAC and AAC values as dependent variables. Results: CAC and AAC were independently associated with age (OR, 95% CI: 2.30 [1.77-2.98] for CAC and 3.48 [2.57-4.73] for AAC), p for difference < 0.001), systolic blood pressure (1.29 [1.08-1.53] and 1.28 [1.07-1.54], p for difference = 0.270), and smoking (1.22, [1.04-1.43] and 1.34 [1.13-1.58]) p for difference = 0.071). Alcohol correlated with AAC only (1.17 [0.97-1.41] for CAC and 1.42 [1.16-1.73] for AAC, p for difference = 0.020). Conclusions: CAC and AAC were associated with similar CVD risk factors. The strength of association slightly differed between CAC and AAC.

BACKGROUND:J waves result mainly from an increased density of transient outward current (Ito ). Mechanical stretch to the heart activates multiple signal transduction pathways, in which Ito may be involved. The purpose of this study was to test the hypothesis that mechanical contact of lung cancer with the heart may manifest J waves.METHODS:We reviewed 12-lead electrocardiograms to examine whether J waves were associated with contact of lung cancer with the heart. J waves were defied as an elevation of ≥0.1 mV at the junction between QRS complex and ST segment with either notching or slurring morphology. The locational interaction between lung cancer and the heart was determined by computed tomography image.RESULTS:A total of 264 patients (176 men; mean 68.5 ± 10.7 years) with lung cancer were evaluated. The prevalence of J waves was 25.4% in the total population. J waves were present in 40 of 44 (90.9%) patients with the contact. In contrast, J waves were present in 25 of 220 (11.4%) patients without the contact. The sensitivity and specificity of the contact for J waves were 90.9% and 88.6%, respectively. The odds ratio of the contact with the heart to the presence of J waves was 78 (95% confidence interval 25.7-236.4). The appearance of J waves that coincided with the development of lung cancer was observed in 12 patients.CONCLUSION:The presence of J waves was associated with the contact of lung cancer with the heart.

Purpose: “Heart Function View (HFV)” is a software that performs phase analysis as well as functional assessment of the left ventricle (LV) using myocardial perfusion single photon emission computed tomography (SPECT) (MPS). Phase analysis-derived phase standard deviation (PhSD) and histogram bandwidth (PhHB) are good indices for detecting LV dyssyncrony. We aimed to examine whether PhHB and/or PhSD (PhHB/PhSD) are useful clinical indicators that reflect the severity of heart failure (HF) in comparison with the LV ejection fraction (EF). Methods: Patients underwent 99m Tc-tetrofosmin quantitative gated MPS including treadmill exercise. In HFV analyses, patients with induced ischemia were excluded. Phase and time-volume curve analyses were performed using HFV (n=66). Results: PhHB/PhSD correlated with LV end-diastolic volume (EDV), end-systolic volume (ESV), the first-third filling fraction (1/3FF), and peak filling rate (PFR) as well as echocardiography tissue Doppler-derived E/e’ as hemodynamic parameters of HF severity. LVEF also correlated with these hemodynamic parameters, except for 1/3FF. PhHB/PhSD positively correlated with log BNP as a neurohumoral marker of HF severity. LVEF negatively correlated with log BNP. PhHB/PhSD negatively correlated with exercise capacity as physiological indicators of HF severity, whereas LVEF did not. PhHB/PhSD were significantly greater in patients receiving cardiac resynchronization therapy (CRT, n=6) than in non-CRT patients (n=66), whereas LVEF were lower. Conclusion: PhHB/PhSD, similar to LVEF, are useful clinical indicators for evaluating HF severity. However, the clinical significance of LVEF and PhHB/PhSD differ. Thus, a phase analysis may additively offer useful information for the management of HF.

Background: Skeletal muscle is important to determine physical activity and exercise capacity in cardiovascular disease. This study aims to investigate the relationship between skeletal muscle volume measured by bioelectrical impedance analysis and ventilation indices assessed by cardiopulmonary exercise test in patients with myocardial infarction.Methods: A total of 60 patients (57 men; 59 +/- 9 years) who underwent percutaneous coronary intervention for ST-elevation myocardial infarction were enrolled into this study. All patients performed cardiac rehabilitation and then achieved physical activity of daily life. No patient was complicated by diabetes mellitus. In symptomlimited cardiopulmonary exercise test, minute ventilation ((V) over dot E), oxygen consumption ((V) over dot O-2), and carbon dioxide production ((V) over dot CO2) were continuously obtained. A volume of skeletal muscle measured by bioelectrical impedance analysis was normalized for height (skeletal muscle index).Results: The skeletal muscle index showed a significant inverse correlation with peak (V) over dot E/(V) over dot O-2 (p = 0.02, r=-0.39) and peak (V)over dot E/(V)over dot CO2 (p= 0.02, r= -0.30). In addition, the skeletal muscle index inversely correlated with (V)over dot E/(V)over dot CO2 slope (p= 0.02, r = -0.30). On the other hand, the skeletal muscle index did not significantly correlate with peak (V) over dot O-2 (p= 0.56, r= 0.08) and peak (V) over dot CO2 (p= 0.99, r= 0.001). Besides, the skeletal muscle index did not significantly correlate with Delta(V) over dot O-2/Delta work rate slope (p = 0.60, r = 0.07).Conclusions: The increase in skeletal muscle index was associated with the amelioration of ventilatory efficacy to exercise at the peak level. Furthermore, the increase in skeletal muscle index may account for favorable prognosis. These findings could strengthen the role of skeletal muscle in exercise capacity of patients with myocardial infarction. (C) 2016 The Authors. Published by Elsevier Ireland Ltd.

Prolonged QRS duration on electrocardiogram (ECG) has been known as a poor prognostic marker. However, little is known about association between progressive intraventricular conduction disturbance and cardiovascular prognosis.From among a database containing 359,737 12-lead ECG recordings, patients whose QRS duration progressively increased from <120 msec to ≥120 msec were selected using software. The prognosis of patients was searched by medical record. The primary endpoint was defined as heart failure hospitalization. The secondary endpoint was heart failure hospitalization, device implantation, or cardiovascular death.A total of 143 patients (100 males; age, 58.9±11.1 years) were enrolled in this study. QRS duration increased by 46.4±13.8 msec, manifesting right bundle branch block (RBBB) in 99 (69.2%) patients and non-RBBB (i.e., left bundle branch block, RBBB with left anterior hemiblock, or nonspecific intraventricular conduction disturbance) in 44 (30.8%). During the follow-up (mean, 16.6±5.3 years), 44 (30.3%), 15 (10.3%), and 6 (4.1%) patients resulted in heart failure hospitalization, device implantation, and cardiovascular death, respectively. Multivariate Cox proportional hazards models revealed that 1) the temporal increase in QRS duration was associated with the primary endpoint (hazard ratio [HR] 1.98; 95% confidence interval [CI] 1.05-3.80; p = 0.04) and the secondary endpoint (HR 2.79; 95% CI 1.55-5.00; p = 0.0001) and 2) the development of non-RBBB was associated with the primary endpoint (HR 3.02; 95% CI 1.59-5.73; p = 0.0001) and the secondary endpoint (HR 2.82; 95% CI 1.57-5.09; p = 0.001).The temporal increase in QRS duration and the development of non-RBBB patterns were independently associated with adverse cardiovascular prognosis.

Long QT syndrome (LQTS) is characterized by an abnormally prolonged QT interval on electrocardiogram and an increased risk of ventricular tachyarrhythmias and sudden cardiac death [ [1] Schwartz P.J. Crotti L. Insolia R. Long-QT syndrome: from genetics to management. Circ. Arrhythm. Electrophysiol. 2012; 5: 868-877 Crossref PubMed Scopus (407) Google Scholar ]. Some clinical and genetic risk factors for arrhythmia events have been identified, but there is not enough evidence for risk stratification for arrhythmia events. Early repolarization is defined as an elevation of J point, either a slurring or notching at the terminal part of QRS complex and has generally been considered benign for decades. However, early repolarization is associated with an increased risk of idiopathic ventricular fibrillation and cardiac death [ 2 Haissaguerre M. Derval N. Sacher F. Jesel L. Deisenhofer I. de Roy L. JL P. Nogami A. Babuty D. Yli-Mayry S. De Chillou C. Scanu P. Mabo P. Matsuo S. Probst V. Le Scouarnec S. Defaye P. Schlaepfer J. Rostock T. Lacroix D. Lamaison D. Lavergne T. Aizawa Y. Englund A. Anselme F. O'Neill M. Hocini M. KT L. Knecht S. GD V. Bordachar P. Chauvin M. Jais P. Coureau G. Chene G. GJ K. Clementy J. Sudden cardiac arrest associated with early repolarization. N. Engl. J. Med. 2008; 358: 2016-2023 Crossref PubMed Scopus (1113) Google Scholar , 3 Tikkanen J.T. Anttonen O. Junttila M.J. Aro A.L. Kerola T. Rissanen H.A. Reunanen A. Huikuri H.V. Long-term outcome associated with early repolarization on electrocardiography. N. Engl. J. Med. 2009; 361: 2529-2537 Crossref PubMed Scopus (644) Google Scholar ]. Furthermore, early repolarization increases the risk of arrhythmia events in other cardiac diseases such as short QT syndrome, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy, and myocardial infarction [ 4 Watanabe H. Makiyama T. Koyama T. Kannankeril P.J. Seto S. Okamura K. Oda H. Itoh H. Okada M. Tanabe N. Yagihara N. Kamakura S. Horie M. Aizawa Y. Shimizu W. High prevalence of early repolarization in short QT syndrome. Heart Rhythm. 2010; 7: 647-652 Abstract Full Text Full Text PDF PubMed Scopus (124) Google Scholar , 5 Naruse Y. Tada H. Harimura Y. Hayashi M. Noguchi Y. Sato A. Yoshida K. Sekiguchi Y. Aonuma K. Early repolarization is an independent predictor of occurrences of ventricular fibrillation in the very early phase of acute myocardial infarction. Circ. Arrhythm. Electrophysiol. 2012; 5: 506-513 Crossref PubMed Scopus (105) Google Scholar ]. In a very recent study, marked early repolarization of ≥0.2 mV was found to be associated with symptoms in patients with LQTS, but early repolarization of ≥0.1 mV (defined with the standard criteria) was not associated with symptoms [ [6] Laksman Z.W. Gula L.J. Saklani P. Cassagneau R. Steinberg C. Conacher S. Yee R. Skanes A. Leong-Sit P. Manlucu J. Klein G.J. Krahn A.D. Early repolarization is associated with symptoms in patients with type 1 and type 2 long QT syndrome. Heart Rhythm. 2014; 11: 1632-1638 Abstract Full Text Full Text PDF PubMed Scopus (24) Google Scholar ]. Thus, we studied the association of early repolarization with cardiac events in a large number of genotype-positive patients with LQTS.

Congenital long QT syndrome (LQTS) is an important cause of sudden cardiac death in young people without any other structural disease. Mutations in the genes encoding the cardiac ion channels or associated proteins have been shown to result in ion channel dysfunction and thereby causing LQTS. We investigated a Japanese family with LQTS for four generations, with the female family members showing severe symptoms. We performed genetic tests for LQTS-related genes and identified a heterozygous KCNH2 mutation (p.K638del). In the family, the KCNH2 mutation had a very high multigenerational inheritance, and female genotype positives showed more severe phenotypes.

BACKGROUND:J wave is known to be associated with increased risk of life-threatening ventricular arrhythmias in both structural and nonstructural heart disease. A documented history of ventricular tachycardia (VT) is also a known predictor for future arrhythmic events. The purpose of this study is to investigate prognostic factors in ventricular tachyarrhythmias in patients with an implanted defibrillator. METHODS:Intracardiac electrograms were thoroughly analyzed in patients with either an implanted implantable cardioverter-defibrillator or with cardiac resynchronization therapy with a defibrillator. The relation between the clinical characteristics and the device interventions for ventricular tachyarrhythmias was evaluated retrospectively with multivariate Cox proportional hazards models. RESULTS:This study enrolled a total of 160 patients who were followed for a mean period of 44 ± 28 months. Of these patients, 31 (19%) showed J wave and 77 (48%) showed documented VT before the device implantation. Multivariate Cox proportional hazards models revealed that the presence of J wave and the documented history of VT before the device implantation were independently associated with device intervention in patients with device implantation even after the adjustment of confounding factors (hazard ratio [HR], 2.90; 95% confidence interval [CI], 1.56-5.24; p=0.001 and HR, 4.34; 95% CI, 2.43-8.05; p<0.0001, respectively). CONCLUSION:The presence of J wave and the documented history of VT prior to device implantation served as independent predictors of future device intervention for ventricular tachyarrhythmias.

Background: Anisotropic and slow conduction in the atrium underlie the development of atrial fibrillation (AF). This study aimed to investigate the P wave characteristics associated with the development of AF in patients with a biphasic P wave in the inferior leads.Methods: Digital analysis of retrospectively recorded 12-lead electrocardiograms was performed to select patients with a biphasic P wave (positive/negative) in lead II from a database of 114,334 patients. Characteristics of the P wave in the inferior leads associated with incidence of AF were determined. Receiver operating characteristic curves dichotomized P wave variables were measured in each lead.Results: A total of 141 patients (77 men; mean age, 64 +/- 19 years) were enrolled in this study. Twenty-nine (20.6%) patients developed AF (AF group) vs. 112 (79.6%) who did not (non-AF group) during a follow-up period of 50 +/- 62 months. The amplitude of the initial P wave portion in lead II was significantly larger in the AF group when compared with the non-AF group (77.3 +/- 77.0 nV vs. 51.0 30.1 nV, p = 0.003), while the amplitude of the terminal P wave portion in lead III was significantly decreased in the AF group when compared with the non-AF group (70.6 +/- 41.3 nV vs. 89.1 +/- 38.1 mu V, p=0.024). The duration of the initial P wave portion in lead III was significantly longer in the AF group when compared with the non-AF group (52.7 +/- 34.6 ms vs. 35.8 +/- 30.4 ms, p=0.011). Multivariate Cox proportional-hazards analysis confirmed that the increased duration of the initial P wave portion in lead III (>= 71 ms) was independently associated with AF development (hazard ratio 2.90, 95% confidence interval 1.16-7.11, p=0.02).Conclusion: The analyses of the biphasic P wave in the inferior leads suggest that the development of AF could be attributed to increased atrial slow conduction. (C) 2015 Japanese Heart Rhythm Society. Published by Elsevier B.V. All rights reserved.

Brugada症候群と早期再分極症候群は，心室細動（VF）を発症し突然死を起こす可能性がある．両症候群は，心電図でST上昇（J波）を認める．その主な機序として，一過性外向き電流（Ito）の増加が考えられている．キニジンに代表されるItoを抑制する薬剤はVFの発生を抑制するとの報告があり，同時にJ波を消失させることも明らかにされている．このような薬剤は，Brugada症候群と早期再分極症候群において植込み型除細動器施行後のVFに対する補助的治療として使用される．本論文では，Brugada症候群と早期再分極症候群に対して有効な薬剤の作用機序を解説し，薬物療法の既報についてまとめる．

BACKGROUND:J wave, or early repolarization has recently been associated with an increased risk of lethal arrhythmia and sudden death, both in idiopathic ventricular fibrillation and in the general population. Hypercalcemia is one of the causes of J point and ST segment elevation, but the relationship has not been well studied. The aim of this study was to examine the effects of hypercalcemia on J point elevation.METHODS:Electrocardiographic findings were compared in 89 patients with hypercalcemia and 267 age- and sex-matched healthy controls with normocalcemia. The association of J point elevation with arrhythmia events in patients with hypercalcemia was also studied.RESULTS:The PR interval and the QRS duration were longer in patients with hypercalcemia than in normocalcemic controls. Both the QT and the corrected QT intervals were shorter in patients with hypercalcemia compared with normocalcemic controls. Conduction disorders, ST-T abnormalities, and J point elevation were more common in patients with hypercalcemia than normocalcemic controls. Following the resolution of hypercalcemia, the frequency of J point elevation decreased to a level similar to that noted in controls. During hospitalization, no arrhythmia event occurred in patients with hypercalcemia.CONCLUSION:Hypercalcemia was associated with J point elevation.

BACKGROUND:P wave ≥0.25mV in inferior leads (P pulmonale) occurs in chronic lung diseases that underlie atrial fibrillation (AF). The purpose of this study was to elucidate the prognostic value of P pulmonale for development of AF. METHODS AND RESULTS:Digital analysis of 12-lead electrocardiogram (ECG) was conducted to enroll patients with P pulmonale from among a database containing 308,391 ECGs. In a total of 591 patients (382 men; 56.4±14.8 years) with P pulmonale (follow-up, 46.7±65.6 months), AF occurred in 61 patients (AF group), but did not occur in 530 patients (non-AF group). Male gender was significantly more prevalent in the AF group than in the non-AF group (80.3% vs. 62.8%, P=0.0047). P-wave duration and PQ interval were significantly longer in the AF group than in the non-AF group (115.4±17.2ms vs. 107.0±17.2ms, P=0.0003 and 166.3±23.9ms vs. 153.2±25.4ms, P=0.0001, respectively). In the total patient group, multivariate Cox proportional-hazards analysis confirmed that male gender (hazard ratio [HR], 2.24; 95% confidence interval [CI]: 1.02-5.49; P=0.045), PQ interval >150ms (HR, 6.89; 95% CI: 2.39-29.15; P<0.0001), and P-wave axis <74° (HR, 2.55; 95% CI: 1.20-5.41; P=0.016) were associated with AF development. In medication-free patients (n=400), only PQ interval >150ms (HR, 9.26; 95% CI: 1.75-170.65; P=0.0055) was independently and significantly associated with AF development. CONCLUSIONS:PQ interval is the strongest stratifier for AF development in P pulmonale.

BACKGROUND:Andersen-Tawil syndrome (ATS) is an autosomal dominant genetic or sporadic disorder characterized by ventricular arrhythmias (VAs), periodic paralyses, and dysmorphic features. The optimal pharmacological treatment of VAs in patients with ATS remains unknown. OBJECTIVE:We evaluated the efficacy and safety of flecainide for VAs in patients with ATS with KCNJ2 mutations. METHODS:Ten ATS probands (7 females; mean age 27 ± 11 years) were enrolled from 6 institutions. All of them had bidirectional VAs in spite of treatment with β-blockers (n = 6), but none of them had either aborted cardiac arrest or family history of sudden cardiac death. Twenty-four-hour Holter recording and treadmill exercise test (TMT) were performed before (baseline) and after oral flecainide therapy (150 ± 46 mg/d). RESULTS:Twenty-four-hour Holter recordings demonstrated that oral flecainide treatment significantly reduced the total number of VAs (from 38,407 ± 19,956 to 11,196 ± 14,773 per day; P = .003) and the number of the longest ventricular salvos (23 ± 19 to 5 ± 5; P = .01). At baseline, TMT induced nonsustained ventricular tachycardia (n = 7) or couplets of premature ventricular complex (n = 2); treatment with flecainide completely (n = 7) or partially (n = 2) suppressed these exercise-induced VAs (P = .008). In contrast, the QRS duration, QT interval, and U-wave amplitude of the electrocardiogram were not altered by flecainide therapy. During a mean follow-up of 23 ± 11 months, no patients developed syncope or cardiac arrest after oral flecainide treatment. CONCLUSION:This multicenter study suggests that oral flecainide therapy is an effective and safe means of suppressing VAs in patients with ATS with KCNJ2 mutations, though the U-wave amplitude remained unchanged by flecainide.

Andersen–Tawil syndrome is a heterogeneous disorder characterized by periodic paralysis, ventricular arrhythmias, QT prolongation, craniofacial dysmorphic features, and autosomal dominant inheritance. Most patients have a mutation in the ion channel gene, KCNJ2, which encodes the inward rectifier K+ channel Kir2.1, a component of the inward rectifier IK1. T-wave alternans, defined as a beat-to-beat change in the amplitude and/or shape on the electrocardiogram (ECG), has been reported as a presage of life-threatening events. Nowadays, measurement of microvoltlevel T-wave alternans that reflects a quantifiable, fundamental electrophysiologic property linked to life-threatening ventricular arrhythmias is a feasible procedure in clinical practice. However, it is not known that T-wave alternans is associated with ventricular arrhythmia in Andersen–Tawil syndrome. It was reported that flecainide was effective in suppressing ventricular tachyarrhythmia in Andersen-Tawil syndrome.1–3 Therefore, we evaluated the effects of flecainide on Twave alternans and ventricular arrhythmia in this syndrome.

Atrial depolarization commences from the sinus node, after which then an impulse propagates from the right atrium to the left atrium. P-waves reflect the electrical depolarization of both the right and left atria. Twelve-lead ECG is ubiquitously used in clinical practice to evaluate patients and provides information regarding the presence of structural heart disease and/or heart rhythm abnormalities. Moreover, P-wave morphological characteristics deserve noting that the pattern of atrial depolarization is normal or ill. P-wave dispersion, as reflected as the interval between the longest and shortest duration of the P-wave in any of the 12-lead ECG leads, is an invariable maker of the incidence and recurrence of atrial fibrillation (AF) (1). Patients with uncontrolled hypertension exhibit a significantly prolonged P-wave duration and increased P-wave dispersion as compared to controls and patients with controlled hypertension (2, 3). Likewise, patients with diabetes display a significantly prolonged Pwave duration and increased P-wave dispersion compared to normal controls (4). Individuals with obesity also have a significantly prolonged P-wave duration and increased Pwave dispersion compared with control s (5, 6). Increased Pwave dispersion is observed among patients with coronary artery disease (7) and dilated or hypertrophic cardiomyopathy (8). The structural remodeling that occurs in these patients can represent P-wave dispersion as an electrophysiological phenotype. Interstitial fibrosis and connexin redistribution in the remodeled atria cause anisotropic conduction and/or discontinuous propagation. In addition, triggered activity, such as early or delayed after depolarization, is prone to occur, thus ensuring the development of AF in the remodeled atrium. QT interval encompasses the time from the earliest activation to the latest repolarization of the ventricular myocardium, and T wave is the result of repolarization gradients within the ventricles of the heart. When ventricular repolarization becomes inhomogeneous, QT dispersion (the difference between the longest and shortest QT interval measured on a 12-lead ECG) is amplified. Although QT interval per se is an invaluable prognostic marker for evaluating whether ventricular arrhythmia occurs (9), QT dispersion has been reported to be a marker for identifying patients at risk for life-threatening arrhythmias after myocardial infarction (10) as well as heart failure (11) and to be associated with cardiovascular mortality in general population (12). Increased QT dispersion has also been linked to increased heterogeneity of ventricular repolarization and is implicated in the genesis of ventricular arrhythmias. It is hypothesized that an important entity underlying QT dispersion is patchy myocardial fibrosis, resulting from myocardial ischemia, ventricular dilatation and neurohormonal activation. It is therefore worth noting that QT dispersion is related to arrhythmogenesis.

Objective To investigate clinical usefulness of a novel program "Heart Function View (HFV)" for evaluating left ventricular (LV) function from myocardial perfusion SPECT (MPS), we compared LV functional parameters (F(x)) calculated by HFV with those obtained by the other similar programs QGS and cardioGRAF or by ultrasound echocardiography (UCG) and examined their correlations with clinical markers of heart failure: plasma BNP concentrations (BNPs) and exercise capacity.Methods Studied patients (n = 60) underwent technetium-99m tetrofosmin quantitative gated MPS including treadmill exercise for examining heart disease. Myocardial stress images were acquired 30 min after the first tracer injection during maximal exercise. Three hours later, the second tracer was injected, and resting images were acquired. LV systolic F(x) [ejection fraction (EF), peak ejection rate (PER)] and diastolic F(x) [first third filling fraction (1/3FF), first third filling rate (1/3FR), peak filling rate (PFR), time to PFR (TPF)] were analyzed, and phase standard deviation (SD) and histogram bandwidth were obtained by phase analysis.Results LV end-diastolic volume (EDV), end-systolic volume (ESV) and EF obtained from HFV were well correlated with those from QGS, cardioGRAF and UCG. A diastolic parameter Doppler E/e' from UCG was significantly with PFR from HFV. There were good correlations between LVEDV, LVESV, LVEF, PER, PFR, 1/3FR, TPF and 1/3FF from HFV and those from cardioGRAF. LVEF, PER, 1/3FR, and PFR were significantly correlated with plasma BNP concentrations. In patients with non-ischemic heart disease (n = 42), phase SD and histogram bandwidth were correlated negatively with exercise capacity or PFR.Conclusions HFV-derived LVF(x) are correlated with LVF(x) from the other programs or UCG, or with the clinical markers of heart failure and are thus useful in the functional assessment for patients with heart disease.